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some higlights.. MS usualy treated by neurologists familiar with immune system but not vascular issues... relative funding ease for studies in autoimmune since MS socienties with the money usually worked with the doctors treating the patients... relative political power within the medical establisment, etc. It rather clearly appears that the resolution between the two competing theories was swung to the autoimmune theory for reasons other than scientifically rigorous testing results in favor of one or the other.

To what is in the article I would add that we created an autoimmune animal model, AEA that had MS like characteristics and because it was a murine animial model gave us the ability to to preclinical testing impossible with only human patients. And of couirse, autoimmune treatment showed hopeful results in AEA (duh ... it was created as an autoimmune model)

This struggle between the two competing theories just a couple decades ago is rather striking since the reaction we seem to be getting from press and from neurologists is that a possible vascular cause is an exotic idea out of left feild and something truely out of the box and unlikely, when it clearly was a strongly competing theory just 20 or thirty years ago!

That is an amazing read. It was like reading the reasons motivating the neuros...but making a case for us demanding an answer to why the current party line stating that this vascular thing is just some big unknown with no connection possible with M.S.
Thanks

It is an amazing article. I am not sure whether it is one of the high rank journals. However, it gives the full support for CCSVI and that the vascular approach is not just "Junk Science" as some people claimed.

It is amazing how the doctors of the 19th century were able to think about MS deeper than what the hi-tech is offering doctors these days. In addition, the Italians were pioneers in the 20th century as well with the treatment of MS and MS-like diseases.

The issues about the validity of the clinical trial was the last weapon for the loosing party back then and now as well.

The main flaw with most of the arguments for immunology MS causes dates back to the 1930s where a clinical trian on animals proven that suppressing the immune system will stop the progress of MS. Logically, this can be refuted because it is stopping a symptom (demyelinating) and not stopping the main cause of the illness. However, people acclaimed this theory with the support of MS societies (and Pharmas behind them) and nobody dared to challenge this theory after that until the 21st century with Zamboni and the others.

Even in the 1970s, financing for any MS research was next to impossible if it does not appeal to the mood of the MS societies. With a lot of public pressure, the MS societies were still reluctant to finance any studies out of the immunology department (does it remind you of the $100k that the Canadian MS society has put for CCSVI???). For example, the Fisher (1978) study has yielded the same results as the immunology test. However, Fisher results were not plausible because it does not get along with the social forces behind the immunology societies controlling all the funding.

This makes it very clear that any breakthrough treatment for MS needs a non-conventional channel. Do not expect the pharma to give it away. Academic labs (who are not aligned with the mood of the societies) can not be funded to work out of the box !!!

Hence, it needs a lot of pushing. The british MS society has seen a lot of public pressure to go in a different direction (documented in this paper) but they were always reluctant and always able to go away with it.

We need to push and push and push until we reach a good level of understanding from all parties that MS threaten lives and not just pockets.

Leaving fundamental research as important as research on human disease and cure to market forces is susceptible to such bias. Recent study on gene mutations in skin and lung cancer diseases being undertaken by a charity organization is a case in point.

[url]The authors interpret their findings to indicate that plaques grow through loss of oligodendrocytes on the plaque border, which is followed by myelin breakdown, scavenging of debris by phagocytes, and infiltration of immune cells such as T cells. What causes the oligodendrocytes to die is not known[/url]

Here's the Barnett and Sutton paper in toto--looking at fresh lesions and cell death preceding myelin loss--the authors propose a few theories. One that has stayed with me is hypoxic injury- because this could be caused by venous hypertension and the inability of oxygen to get into the MS brain in a timely matter, due to the delayed exit of deoxygenated blood. Endothelial disruption and a break in the BBB could follow.

Oligodendrocytes, and to a lesser extent other cell types in the outer lesion edge and the outermost rims of preserved myelin in expanding concentric lesions, showed intense expression of markers of hypoxia-like tissue damage (D-110epitope), regulators in the induction of hypoxic preconditioning (HIF-1a) and stress proteins which afford protection against hypoxic injury (heat-shock protein 70). Mitochondrial dysfunction, perhaps induced by inﬂammatory mediators or nitrogen/oxygen intermediates,has been invoked as the potential basis of preconditioning.

the idea I had was that apoptosis caused the cell death. apoptosis is programmed cellular suicide. When humans are in the womb for example, we have webbed fingers. Those cells are programmed to disappear before birth. If this same mechanism was broken, cells could get the wrong programs, causing cell death.

Hypoxia fits just as well as far as I know, and it would fill out this model well. So ccsvi-> hypoxia->oligodendracite death->immune response.

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